Left ventricular (LV) diastolic dysfunction is a common problem among patients with a wide range of cardiovascular diseases. For a number of conditions, notably hypertension (particularly if associated with LV hypertrophy), myocardial ischemia or infarction, and valvular heart disease (particularly aortic stenosis), LV diastolic dysfunction may occur relatively early in the disease process. LV diastolic dysfunction may occur in patients with systolic dysfunction but, importantly, can also occur in the setting of preserved LV systolic function. For example, approximately 50% of patients presenting with acute pulmonary edema have normal systolic function on two-dimensional (2-D) echocardiography, and in many of these cases, the underlying cause may be LV diastolic dysfunction. This is now commonly referred to as “heart failure with preserved LV ejection fraction.” Assessment of LV diastolic function is now a standard part of a comprehensive echocardiogram, and guidelines for the assessment of LV diastolic function have been published.
Patients presenting for cardiac surgery are at risk of diastolic dysfunction or frank diastolic heart failure, and this may be responsible for, or contribute to, perioperative hemodynamic instability. The main risk factors and clinical features are outlined in Table 8-1 . The echocardiographic assessment of diastolic function primarily involves the interpretation of transmitral, pulmonary venous, and mitral annular tissue Doppler. A careful, systematic assessment of LV diastolic filling can be undertaken but should be interpreted in the context of the individual patient, considering cardiac structure or function and hemodynamics. This chapter outlines the application of these techniques to the practice of perioperative TEE.
| Risk Factors | Clinical Features |
|---|---|
| Advancing age (>65 yrs) Female gender Renal failure Diabetes Hypertension Aortic stenosis LV hypertrophy Coronary artery disease | History of acute pulmonary edema A gallop rhythm with a fourthheart sound Radiographic evidence of pulmonary congestion and normal heart size ECG evidence of LV hypertrophy Normal or increased ejection fraction Increased end-diastolic pressure on preoperative angiogram |
The physiology of diastole
The phases of diastole
The pressure changes in the left atrium (LA) and the LV and the volume change in the left ventricle throughout the cardiac cycle are shown in Figure 8-1 . Diastole extends from closure of the AV to closure of the MV and is composed of four phases:
- 1.
isovolumetric relaxation
- 2.
early filling
- 3.
diastasis
- 4.
atrial systole
Many factors influence ventricular filling during these phases, but in the end, the LA-to-LV pressure gradient is the driving force for ventricular filling.
Isovolumetric relaxation
Isovolumetric relaxation commences with closure of the AV and extends to opening of the MV. Ventricular volume remains unchanged, and there is a rapid fall in intracavity pressure due to active relaxation. The (IVRT) is prolonged in any condition that impairs active relaxation (e.g., myocardial ischemia); it is shortened by a raised LA pressure, because this causes earlier opening of the MV.
Early diastolic filling
Early diastolic filling begins with opening of the MV. Ventricular pressure continues to decline despite ventricular filling because of ongoing active relaxation. The pressure gradient from the left atrium to the left ventricle is greatest during this phase, resulting in as much as 80% of ventricular filling. The main determinants of diastolic filling at this time are the rate of active relaxation, the recoil of the elastic myocardial elements, and the LA pressure. Early diastolic filling can be characterized (invasively) by the dV/dt).
Diastasis
Ventricular filling slows in mid-diastole as the transmitral pressure gradient declines. This phase is known as diastasis and is perhaps the most complicated phase of diastole. The main determinant of ventricular filling at this time is LV chamber compliance (dV/dP) or its inverse, chamber stiffness (see Figure 8-1 ).
Chamber compliance is determined by a number of factors, including intrinsic myocardial stiffness, ventricular mass, pericardial restraint, RV volume, and loading conditions. Chamber compliance is also a function of ventricular volume; a distended chamber has a lower compliance than an empty one. Loading conditions and ventricular mass may affect chamber compliance without altering myocardial stiffness.
Atrial systole
Atrial systole increases the transmitral pressure gradient and under normal circumstances accounts for 15% to 20% of ventricular filling. In conditions that impair active myocardial relaxation, such as aortic stenosis, the contribution of atrial systole to ventricular filling may increase substantially.
Active versus passive diastolic dysfunction
Abnormalities of diastole can be divided into those affecting the early, active part of relaxation and those affecting the later, passive filling phases. Active diastolic dysfunction is due to delayed reuptake of calcium ions into the sarcoplasmic reticulum and causes prolongation of relaxation, which affects isovolumetric relaxation and the first part of early filling. Passive diastolic dysfunction is due to reduced chamber compliance (or increased chamber stiffness) and affects the later part of early filling, diastasis, and atrial systole. Most forms of diastolic dysfunction in their early clinical course are of the abnormal relaxation type (e.g., myocardial ischemia, hypertension, aortic stenosis, and hypertrophic cardiomyopathy). Reduced chamber compliance is the predominant finding in infiltrative processes (e.g., amyloidosis) and myocardial fibrosis (e.g., widespread myocardial infarction). The natural history of diastolic dysfunction is that, with time, as the disease advances, abnormal relaxation progresses to reduced chamber compliance and increased stiffness.
Echocardiographic assessment of left ventricular diastolic dysfunction
The major physiologic abnormality resulting from abnormal diastolic function is elevated LV filling pressure. The echocardiographic assessment of LV diastolic dysfunction is largely based on the careful and systematic assessment of the transmitral, pulmonary venous, and mitral annular PW Doppler waveforms. Color M mode may also be useful. Importantly, the information regarding LV diastolic dysfunction should be integrated with that of systolic LV function and LV volume status that can be obtained from 2-D imaging. In general, reliance on only one echo-Doppler variable should be avoided; instead, careful integration of all available information should be made in context with the patient’s clinical status, particularly hemodynamics.
2-D imaging
LV hypertrophy is a frequent finding in patients with diastolic dysfunction. Ventricular hypertrophy can be either concentric (wall thickness increased out of proportion to chamber size) or eccentric (wall thickness increased in proportion to the increase in chamber size). LV pressure overload (from aortic stenosis or hypertension) produces concentric hypertrophy and is associated with impaired relaxation and, eventually, reduced chamber compliance. Reduced LV compliance associated with LV hypertrophy may contribute to hemodynamic instability during the perioperative period. Volume overload (from mitral and aortic regurgitation) produces eccentric hypertrophy. Concentric hypertrophy may be asymmetrical, frequently involving the anterior septum in preference to other segments (the basal “knuckle” seen in elderly hypertensive patients).
With transesophageal echocardiography (TEE), LV hypertrophy can be assessed by measurement of ventricular wall thickness at end diastole in the transgastric mid-short-axis view using either 2-D or M-mode imaging (see Chapter 7 ). Hypertrophy of the anterior septum is best appreciated in the midesophageal long-axis view. With TEE, it is difficult to avoid obliquely imaging the anterior septum using M mode; therefore, 2-D measurements should be used. Normal values for LV wall thickness are provided in Appendix 3 . Scrutiny of the preoperative echocardiogram (where available) may avoid the need for more detailed assessment of the presence of LV hypertrophy during a perioperative TEE.
In patients with severe diastolic dysfunction or mitral stenosis, prolonged diastolic filling can be appreciated on 2-D imaging. A presystolic “kick” may be observed due to atrial systole.
LA size is an important marker of the severity of LV diastolic dysfunction. An LA volume of 34 mL/m (reflective of moderate or greater LA dilatation ) has been shown to predict death and nonfatal cardiovascular events among patients without atrial fibrillation or valvular heart disease. The most accurate echocardiographic measurement of LA size is the LA volume from the transthoracic apical views. LA size is generally underestimated when assessed with TEE ; thus, TEE values need to be interpreted carefully. Preoperative data on LA size may reflect longer-term diastolic dysfunction and thus increase the likelihood of diastolic dysfunction occurring in the perioperative period. LA enlargement also occurs in the absence of LV diastolic dysfunction in patients with atrial arrhythmias and valvular heart disease, particularly mitral stenosis.
Pulse wave Doppler imaging
Ventricular filling depends on the LA-to-LV pressure gradient, which also determines the transmitral diastolic velocity profile. For this reason, the transmitral PW Doppler waveform has become an important tool in the assessment of diastolic function. As the transmitral pressure gradient is also influenced by atrial filling, additional information is gained by evaluation of the pulmonary venous PW Doppler waveform. A number of comprehensive reviews deal with the PW Doppler evaluation of diastolic function.
Transmitral pulse wave Doppler waveforms
Following isovolumetric relaxation and opening of the MV, diastolic filling commences. The normal transmitral velocity waveform consists of two peaks; a larger E wave due to early diastolic filling and a smaller A wave due to atrial systole. A number of variables can be measured from the Doppler signal, including the IVRT, E max , E wave VTI (the area under the velocity–time curve), E wave deceleration time, maximum A wave velocity (A max ), A wave VTI, and the ratio of E to A ( Figure 8-2 ; reference values are provided in Table 8-2 ). While these variables can readily be assessed, the most common and practical approach to the transmitral Doppler is to consider patterns of abnormal transmitral flow and to integrate this with information from the mitral annular tissue, pulmonary venous, or both Doppler waveforms. The characteristic patterns of transmitral Doppler are impaired relaxation, pseudonormalization, and restrictive filling.
| Parameter | Normal (Approximate Range) | Abnormal Relaxation | Pseudonormal | Restrictive |
|---|---|---|---|---|
| IVRT (m/sec) | 60-100 | Increased | Decreased | Decreased |
| Transmitral E max (m/sec) | 0.5-1.0 (<30 yrs) 0.4-0.7 (>60 yrs) | Decreased | Normal | Increased |
| Transmitral A max (m/sec) | 0.2-0.5 (<30 yrs) 0.4-0.7 (>60 yrs) | Increased | Normal | Decreased |
| E/A ratio | 1.0-3.0 (<30 yrs) 0.7-1.3 (>60 yrs) | <1 | 1-2 | >2 |
| E dec (m/sec) | 160-200 (<30 yrs) 170-240 (>60 yrs) | >220 | 150-200 | <150 |
| PV S wave | 0.3-0.6 (<30 yrs) 0.5-0.8 (>60 yrs) | Increased | Decreased | Decreased |
| PV D wave | 0.5-0.8 (<30 yrs) 0.3-0.6 (>60 yrs) | Decreased | Increased | Increased |
| S/D ratio | 0.5-1.0 (<30 yrs) 1.0-2.0 (>60 yrs) | >1 | <1 | <1 |
| Pulmonary venous reversed A wave (m/sec) | 0.1-.03 (<30 yrs) 0.2-0.4 (>60 yrs) | <0.35 | >0.35 | <0.35 |
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